Article
Mixed responses to targeted therapy driven by chromosomal instability through p53 dysfunction and genome doubling.
Nature communications - 13 Jun 2024
Hobor Sebastijan, Al Bakir Maise, Hiley Crispin T, Skrzypski Marcin, Frankell Alexander M, Bakker Bjorn, Watkins Thomas B K, Markovets Aleksandra, Dry Jonathan R, Brown Andrew P, van der Aart Jasper, van den Bos Hilda, Spierings Diana, Oukrif Dahmane, Novelli Marco, Chakrabarti Turja, Rabinowitz Adam H, Ait Hassou Laila, Litière Saskia, Kerr D Lucas, Tan Lisa, Kelly Gavin, Moore David A, Renshaw Matthew J, Venkatesan Subramanian, Hill William, Huebner Ariana, Martínez-Ruiz Carlos, Black James R M, Wu Wei, Angelova Mihaela, McGranahan Nicholas, Downward Julian, Chmielecki Juliann, Barrett Carl, Litchfield Kevin, Chew Su Kit, Blakely Collin M, de Bruin Elza C, Foijer Floris, Vousden Karen H, Bivona Trever G, Hynds Robert E, Kanu Nnennaya, Zaccaria Simone, Grönroos Eva, Swanton Charles
Abstract excerpt
The phenomenon of mixed/heterogenous treatment responses to cancer therapies within an individual patient presents a challenging clinical scenario. Furthermore, the molecular basis of mixed intra-patient tumor responses remains unclear. Here, we show that patients with metastatic lung adenocarcinoma harbouring co-mutations of EGFR and TP53, are more likely to have mixed intra-patient tumor responses to EGFR...
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